This research project is designed to investigate several metabolic parameters relating to ovulation of the ovarian follicle oftherabbit. Previous studies have demonstrated an initial cessation in follicular steroid synthesis prior to ovulation. The experiments were designed to measure the in vitro synthesis and metabloism of protein, RNA, and sterols in this same preovulatory interval Experiments were performed to measure the receptor binding of gonadotropin in the same interval to determine whether a failure to bind the stimulating agent could account for the observed cessation in preovulatory follicular function. In the first series of experiments, whole follicles were obtained from rabbits mated 0, 2, 6, or 12 hours previously and the capacity to incorporate radioactive amino acids into protein measured. Incorporation rates were found to peak at 6 hours postcoitus and drop to control levels at 12 hours after mating. In other studies, follicles from unmated rabbits responded to luteinizing hormone (LH) in vitro, but neither FSH nor cyclic AMP exerted an vitro stimulation of protein synthesis. While amino acid incorporatio into protein by follicles increased in the preovulatory interval, the inocrporation of radioactive uridine into RNA remained unchanged over this same time interval. Follicles isolated 2, 6, and 12 hours postcoitus incorporated no more precursor into RNA than did follicles from unmated rabbits. Furthermore, LH did not stimulate increased precursor incorporation into RNA in follicles from unmated rabbits; FSH and cyclic AMP did increase uridine incorporation. The protein and RNA experiments suggest that the preovulatory interval is marked by a transitory increase in protein synthesis accompanied by little or no new RNA synthesis. In the second seriess of studies, the specific binding of gonadotropin to follicles has been measured. No change in the affinity of the follicles for HCG in the 10-12 hour period between mating and ovulation could be observed in follicles obtained from unmatedrabbits. This finding suggest that the preovulatory metabolic cessation cannot be totally attributed to a decline in the capacity of follicular tissue to bind the stimulatory gonadotropin.